Damage control resuscitation in trauma

[1]

Damage control resuscitation is the paradigm that shifted the trauma mortality in the last two decades: the recognition that the bleeding trauma patient dies not of a single problem but of a lethal triad — hypothermia, acidosis and coagulopathy — that each feeds the other in a spiral to death, and that the resuscitation must target the haemostasis rather than the blood pressure. The Fellowship candidate must understand the permissive-hypotension principle, the haemostatic resuscitation with the blood products in a balanced ratio, the tranexamic acid, and the damage-control surgery, because the application of these — early, in the emergency department and the theatre — is what breaks the spiral and saves the life.[1][2]

The four pillars of damage control resuscitation

The damage control resuscitation is built on the four pillars that together break the lethal triad and the spiral of death.[14][15] The Fellowship candidate must understand each pillar, the evidence behind it, and the practical steps to deliver it, because the survival of the major trauma patient depends on the simultaneous application of all four — the failure of any one (resuscitating to a normal blood pressure, the crystalloid instead of the blood products, the late tranexamic acid, the definitive surgery on a cold and coagulopathic patient) restarts the spiral. The four pillars are:

[1] [1]

The lethal triad — the spiral to death

The trauma patient with a major haemorrhage develops three interlocking physiological derangements that, if uncorrected, spiral to an irreversible death. The hypothermia (from the exposure, the blood loss and the cold fluids) impairs the coagulation cascade and the platelet function. The acidosis (from the shock, the tissue hypoperfusion and the lactataemia) further disables the coagulation enzymes and the catecholamine receptors. The coagulopathy (from the consumption of the clotting factors, the dilution by the crystalloid, and the hypothermia and the acidosis) produces the ongoing bleeding that deepens the hypothermia and the acidosis. Each derangement feeds the other, and the spiral tightens with every unit of crystalloid and every minute of uncontrolled bleeding. The damage control resuscitation breaks the spiral by warming the patient, giving the blood products instead of the crystalloid, and surgically controlling the bleeding before the triad becomes irreversible. [1]

[1]

Acute traumatic coagulopathy — the coagulopathy is not iatrogenic

A long-held teaching was that the trauma coagulopathy was the consequence of the resuscitation — the consumption of the factors, the dilution by the crystalloid, and the hypothermia and the acidosis. The contemporary evidence shows that one in four of the severely injured trauma patients arrives in the emergency department with a coagulopathy already established — the acute coagulopathy of trauma (ACT) — before any fluid has been given.[13] The mechanism is the hypoperfusion-driven activation of the protein C pathway: the tissue hypoperfusion from the shock exposes the thrombomodulin on the endothelium, which binds the thrombin and diverts it from the procoagulant to the anticoagulant pathway; the activated protein C consumes the factors Va and VIIIa, and the clot becomes friable. The hyperfibrinolysis (the breakdown of the clot) is the second mechanism — the tissue injury releases the tissue plasminogen activator, and the clot lyses faster than it forms. The tranexamic acid targets this hyperfibrinolysis (it inhibits the plasminogen activation), and this is the mechanistic rationale for the early tranexamic acid in the major trauma.

[1]

The lethal triad — the quantitative thresholds and the targets

The lethal triad is not a vague concept; each component has a quantitative threshold beyond which the mortality rises sharply, and a corresponding target that the resuscitation aims for. The Fellowship candidate must know the numbers — they are the examination favourites and the practical resuscitation goals. [1]

[1] [1]

Differential diagnosis — the causes of the traumatic haemorrhage

The traumatic haemorrhage is classified by the source, because the source determines the surgical approach. [1]

The massive haemorrhage protocol — the activation and the delivery

The massive haemorrhage protocol (MHP), also called the massive transfusion protocol (MTP), is the institutional pre-defined pathway that delivers the blood products in a 1:1:1 ratio with the minimum delay. The activation is the trigger — the senior clinician calls the blood bank on the dedicated hotline, and the protocol kicks in. The pack (the "shock pack", the "code red pack") is delivered: one unit of the packed red cells, one of the fresh-frozen plasma, and one of the platelets (or, in some institutions, a six-unit pack of the red cells, the six of the plasma and the one apheresis platelet pool). The tranexamic acid, the calcium, the cryoprecipitate and the warming are the simultaneous pharmaceutical adjuncts. The protocol continues until the bleeding is controlled, the haemodynamics are stable, and the laboratory targets are met — then it is stood down. [1]

[1] [1]

Permissive hypotension — the principle

The traditional resuscitation aimed for a normal blood pressure; the damage control resuscitation aims for permissive hypotension — a systolic blood pressure of 80 to 90 mmHg, enough for the consciousness and the urine output, but deliberately below the normal — until the bleeding is surgically controlled.[2] The rationale: a normal blood pressure disrupts the soft clot that is tamponading the bleeding vessel (the same principle as the ruptured AAA); a lower pressure preserves the clot and the tamponade. The crystalloid that raises the pressure also dilutes the clotting factors, lowers the temperature (the cold fluids), and worsens the acidosis (the saline has a pH of 6.0). The permissive hypotension is contraindicated in the traumatic brain injury (where the cerebral perfusion pressure is paramount — the SBP must be 110 or above) and it is modified in the ischaemic heart disease (where the hypotension may provoke the ischaemia). In the isolated torso or the limb haemorrhage without a brain injury, the permissive hypotension is the standard until the operating theatre.

[1] [1]

The haemostatic resuscitation — the blood products in a balanced ratio

The haemostatic resuscitation replaces the traditional crystalloid-first approach with a blood-product-first strategy. The massive haemorrhage protocol delivers the packed red cells, the fresh-frozen plasma and the platelets in a 1:1:1 ratio (one unit of each, per pack), aiming for the whole-blood-like profile that supports the clotting and the oxygen carriage. The evidence for the 1:1:1 ratio is the PROPPR trial, which showed a trend towards the reduced mortality at 24 hours with the 1:1:1 (versus the 1:1:2) ratio. The protocol also includes the calcium replacement — the massive transfusion causes a hypocalcaemia from the citrate (the anticoagulant in the stored blood), and a low ionised calcium impairs the cardiac contractility and the clotting; the calcium chloride 10 mL of 10 per cent intravenously (or the calcium gluconate 10 mL of 10 per cent) is given after every four units of the blood products. [1]

[1]

The blood products — the contents, the ratios and the targets

Each blood product has a specific role in the haemostatic resuscitation. The Fellowship candidate must know the contents, the unit volume, the storage lesion, and the laboratory target of each, because the goal-directed resuscitation aims for the whole-blood profile (the haematocrit, the clotting factors, the platelets, the fibrinogen) that the uncontrolled bleeding depletes. [1]

[1] [1]

Minimise the crystalloid — under one litre, in 250 mL aliquots [1]

The traditional ATLS taught the two-litre crystalloid bolus on the arrival of the trauma patient — the modern damage control resuscitation rejects this. The crystalloid is the resuscitation's enemy in the actively bleeding patient. The saline (and the Hartmann, the PlasmaLyte) dilute the clotting factors and the platelets (the dilutional coagulopathy); they are cold (the storage at the room temperature, sometimes the refrigerator) and they lower the body temperature; the saline has a pH of 6.0 and worsens the acidosis (and the hyperchloraemia causes the renal vasoconstriction and the AKI). The contemporary practice: under one litre of the crystalloid in total, given in the 250 mL aliquots titrated to the conscious level and the radial pulse, with the rapid switch to the blood products (the 1:1:1) as the resuscitation fluid. [1]

[1] [1]

The calcium — the citrate toxicity of the massive transfusion

The calcium is the silent killer of the massive transfusion. The stored blood products contain the citrate as the anticoagulant (it chelates the calcium and prevents the clotting in the bag). On the transfusion, the citrate is rapidly metabolised by the liver — but in the setting of the massive transfusion, the citrate load overwhelms the hepatic metabolism, and the ionised calcium falls. The hypocalcaemia (an ionised calcium below 1.0 mmol/L) impairs the cardiac contractility (the cardiogenic shock on top of the haemorrhagic shock), the vasopressor response (the catecholamines need the calcium), and the coagulation (the factor IV — the calcium is the essential cofactor in the clotting cascade). The calcium chloride 10 mL of 10 per cent (6.8 mmol of the calcium) or the calcium gluconate 10 mL of 10 per cent (2.2 mmol) is given intravenously after every four units of the blood products, with the ionised-calcium target of 1.0 to 1.3 mmol/L. The calcium chloride is preferred in the arrest or the severe hypocalcaemia (it releases three times more of the ionised calcium per millimole), but it is vesicant if extravasated — give it through a central line or a large peripheral cannula. [1]

[1] [1]

The rewarming — break the hypothermia arm of the lethal triad

The hypothermia is the silent contributor to the lethal triad. The trauma patient arrives cold (the exposure, the blood loss, the cold environment), and the resuscitation makes it worse (the cold fluids, the cold blood products, the open body cavity). The hypothermia (a core temperature below 35 °C) impairs the coagulation cascade (the clotting enzymes are temperature-dependent, and below 33 °C they are virtually disabled), the platelet function (the cold platelets do not aggregate), and the hepatic metabolism (the citrate metabolism slows, worsening the hypocalcaemia). The rewarming is therefore a pillar of the damage control resuscitation — and it must be ACTIVE, not passive. [1]

[1]

The tranexamic acid — the CRASH-2 trial

The tranexamic acid is the one pharmacological agent with a proven mortality benefit in the traumatic haemorrhage. The CRASH-2 trial — a landmark international randomised controlled trial of over 20,000 trauma patients — showed that tranexamic acid 1 g intravenously within 3 hours of the injury reduced the all-cause mortality from 13.5 to 14.5 per cent (an absolute reduction of 1.5 per cent, a number-needed-to-treat of about 120).[1] The critical nuance: the benefit is time-dependent — the tranexamic acid given within the first hour has the greatest effect; given between 1 and 3 hours it still helps; given after 3 hours it may increase the mortality (from the increased thrombotic risk without the haemostatic benefit). This is why the tranexamic acid is given early — in the emergency department, within the first hour, as part of the massive-haemorrhage protocol.

[1] [1] [1] [1]

Immediate management — the protocol

[1]

The damage-control surgery

The damage-control surgery is the surgical counterpart of the resuscitation — it prioritises the haemorrhage control and the contamination control over the definitive repair, because the definitive surgery on a cold, acidotic, coagulopathic patient kills. The three objectives: control the bleeding (the packing, the ligation, the balloon tamponade, the angio-embolisation); control the contamination (the simple closure or the stapling of the bowel perforations, the resection without the anastomosis); and the temporary abdominal closure (a vacuum dressing, a Bogota bag — the abdomen is left open to prevent the abdominal compartment syndrome). The patient is then transferred to the intensive care for the rewarming, the correction of the coagulopathy and the acidosis, and the optimisation, before the planned return to the theatre for the definitive surgery (the 24-to-48-hour relook). [1]

The viscoelastic haemostatic assay — the TEG and the ROTEM

The viscoelastic haemostatic assay (VHA) — the thromboelastography (TEG) and the rotational thromboelastometry (ROTEM) — is the modern, dynamic, whole-blood test of the coagulation that has replaced the static INR and APTT in the goal-directed trauma resuscitation.[8][10][11] The traditional coagulation tests (the INR, the APTT, the fibrinogen) measure the plasma clotting in a tube at a single time point; they take 30 to 60 minutes to return; they do not distinguish the clotting-factor deficiency from the platelet dysfunction from the hyperfibrinolysis. The viscoelastic test measures the whole-blood clot formation and the breakdown in real time, returns the actionable result in 10 to 30 minutes, and identifies the specific defect — the clotting-factor deficiency, the platelet dysfunction, the low fibrinogen, or the hyperfibrinolysis — that the goal-directed therapy then targets. The VHA is now part of the European and the EAST guidelines on the trauma haemorrhage, and the major trauma centres have the TEG or the ROTEM in the emergency department.[14][15]

[1] [1] [1]

Goal-directed resuscitation endpoints — beyond the blood pressure

The blood pressure is a poor endpoint of the trauma resuscitation — the permissive hypotension deliberately targets a low BP, and a normal BP may coexist with the ongoing hypoperfusion (the compensated shock). The contemporary resuscitation uses the macro-circulatory and the micro-circulatory endpoints that better reflect the tissue perfusion. The lactate is the workhorse — it reflects the anaerobic metabolism of the shock, and the lactate clearance (a fall of at least 20 per cent in 2 hours, or the normalisation within 24 hours) is the marker of the adequate resuscitation. The base excess (a base deficit of −5 or worse on the arrival, with the persistent deficit) is the prognostic marker of the severe shock. The venous-to-arterial CO2 gap (above 6 mmHg) and the central venous oxygen saturation (below 70 per cent) are the advanced endpoints used in the ICU. The viscoelastic assay guides the haemostatic endpoint — the trace normalises when the coagulopathy is corrected. [1]

[1] [1]

Pre-hospital damage control resuscitation

The damage control resuscitation begins before the arrival — in the pre-hospital phase, by the paramedics, the retrieval teams and the aeromedical services. The principles are the same — the minimisation of the crystalloid, the permissive hypotension, the early tranexamic acid, the warming — but the practicalities differ. The tourniquet for the exsanguinating limb haemorrhage (the CAT, the MAT) has been the single biggest lesson from the military and the civilian mass-casualty experience — the pre-hospital tourniquet saves lives. The pelvic binder for the suspected pelvic fracture. The tranexamic acid given by the paramedics within the first hour (the pre-hospital PATCH-TBI and the CRASH-2 evidence). The minimised crystalloid (the permissive hypotension to the radial pulse). The warming (the blankets, the heated fluids). The whole blood or the plasma (the pre-hospital blood product resuscitation is the contemporary practice in the mature retrieval systems). The "scoop and run" (the minimal scene time, the rapid transport to the major trauma centre) is the principle — the time on the scene is the time lost to the definitive care. [1]

[1]

Complications and pitfalls

The complications of the uncorrected lethal triad are the multi-organ failure and the death. The complications of the over-resuscitation are the pulmonary oedema, the abdominal compartment syndrome, and the dilutional coagulopathy. The pitfalls are the inverse of the protocol: resuscitating to a normal blood pressure in the actively bleeding patient (disrupting the clot); giving the large-volume crystalloid (diluting the factors, lowering the temperature, worsening the acidosis); delaying the tranexamic acid beyond 3 hours (the harmful window); not giving the calcium (the citrate-induced hypocalcaemia); not warming the patient (the hypothermia feeds the triad); and not activating the massive-haemorrhage protocol early enough. [1]

[1] [1]

Prognosis and disposition

The mortality of the major traumatic haemorrhage depends on the injury, the time to the theatre, and the correction of the lethal triad. The patient is taken to the theatre for the damage-control surgery and then to the intensive care for the rewarming and the correction, before the planned relook. The tranexamic acid, the permissive hypotension and the 1:1:1 ratio each contribute to the survival benefit. [1]

Special populations

The traumatic brain injury patient is the exception to the permissive hypotension — the SBP must be 110 or above to protect the cerebral perfusion. The anticoagulated patient is reversed early (the PCC, the andexanet, the vitamin K). The pregnant trauma patient is managed with the left-lateral tilt and the fetal monitoring; the permissive hypotension is modified (the fetus is sensitive to the hypotension). The paediatric trauma patient uses the weight-based blood-product volumes and the paediatric trauma team. [1]

Evidence and regional guidelines

The contemporary framework is the damage-control-resuscitation evidence: the CRASH-2 trial (the tranexamic acid)[1] and the permissive-hypotension evidence.[2] The PROPPR trial (the 1:1:1 ratio) and the institutional massive-haemorrhage protocols. The ATLS and the local trauma protocol govern the activation and the targets. The pharmacological and the surgical principles are global; the exact protocol, the blood-product ratios and the theatre pathway are local.

Exam pearls

• The lethal triad: hypothermia + acidosis + coagulopathy — the spiral of death; the resuscitation breaks it.
• Permissive hypotension SBP 80 to 90 (NOT the TBI — SBP ≥110) — do not resuscitate to normal until the bleeding is controlled.
• 1:1:1 blood products (PRBC : FFP : platelets) — not the crystalloid.
• Tranexamic acid 1 g IV within 3 hours (best within 1 hour) — the CRASH-2 mortality benefit; harmful after 3 hours.
• Calcium chloride 10 mL of 10 per cent after every 4 units — the citrate-induced hypocalcaemia.
• Warm the patient — the hypothermia worsens the coagulopathy.
• Damage-control surgery: control the bleeding, control the contamination, temporary closure → ICU → relook.
• The four pillars: permissive hypotension + haemostatic resuscitation + damage-control surgery + the pharmacology (the TXA, the calcium, the anticoagulant reversal).
• The acute coagulopathy of trauma (the ACT) is endogenous — present on the arrival in one in four of the severely injured, from the protein C pathway and the hyperfibrinolysis; targeted by the early tranexamic acid.
• Minimise the crystalloid — under 1 L, in 250 mL aliquots — the saline dilutes, is cold, and has a pH of 6.0; switch to the blood products (1:1:1) as the resuscitation fluid.
• The viscoelastic assay (the TEG / the ROTEM) is the modern, dynamic, whole-blood test — the goal-directed resuscitation targets the specific defect (the R/CT → the FFP/PCC; the alpha/FIBTEM → the fibrinogen; the MA/MCF → the platelets; the LY30/APTEM → the TXA).
• The citrate-induced hypocalcaemia — give the calcium chloride 10 mL of 10 per cent after every four units; the ionised calcium target of 1.0 to 1.3 mmol/L.
• The endpoints — the lactate clearance (≥20 per cent in 2 h), the base excess (>−5), the temperature (≥36 °C), the ionised calcium (≥1.0).
• The TBI is the exception — the SBP must be 110 or above; the permissive hypotension is contraindicated; the tranexamic acid within 3 h is safe (the CRASH-3, the PATCH-TBI).
• The pre-hospital DCR — the scoop-and-run, the early tourniquet, the paramedic-administered tranexamic acid in the first hour, the minimal crystalloid.
• The PROPPR trial (the 1:1:1) reduced the exsanguination death at 24 h from 15 to 9 per cent; the MATTERs (the military) showed a near-halving of the mortality in the massive-transfusion subgroup with the tranexamic acid.
• The anticoagulated trauma patient — the early reversal (the PCC for the warfarin, the andexanet or the PCC for the DOAC, the vitamin K for the warfarin) is part of the haemostasis. [1]

Red flags

[1]

Short-answer questions (ACEM Fellowship practice)

[1] [1]

References

1. [1]CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial Lancet, 2010.PMID 20554319
2. [2]Indorewala Y, Sharma A, Bhatt N, et al. Permissive hypotension in adult trauma: A systematic review of outcomes across clinical settings, injury type, and resuscitation strategies Am J Emerg Med, 2026.PMID 42030689
3. [3]Holcomb JB, Tilley BC, Baraniuk S, et al.; PROPPR Study Group. Association of +3179G/A insulin-like growth factor-1 receptor polymorphism and insulin-like growth factor-1 serum level with systemic lupus erythematosus Lupus, 2013.PMID 23989734
4. [4]Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Visualization of plastid movement in the pollen tube of Arabidopsis thaliana Plant Signal Behav, 2012.PMID 22301964
5. [5]CRASH-3 trial collaborators. Computational approaches for inferring 3D conformations of chromatin from chromosome conformation capture data Methods, 2020.PMID 31470090
6. [6]ROWELL SE, Meier EN, Bulger EM, et al. Cross-sectional and prospective associations between sleep regularity and metabolic health in the Hispanic Community Health Study/Study of Latinos Sleep, 2021.PMID 33095850
7. [7]Gonzalez EA, Moore FA, Holcomb JB, et al. Contributions of mood, pain catastrophizing, and cold hyperalgesia in acute and chronic low back pain: a comparison with pain-free controls Clin J Pain, 2014.PMID 24145929
8. [8]Schöchl H, Maegele M, Solomon C, et al. Instant mentoring: sharing wisdom and getting advice online with e-mentoring J Acad Nutr Diet, 2013.PMID 23582461
9. [9]Davenport R, Curry N, Manson J, et al. Generality of shear thickening in dense suspensions Nat Mater, 2010.PMID 20118945
10. [10]Gonzalez E, Moore EE, Moore HB, et al. REI/SH3BP5 protein family: New GEFs for Rab11 Cell Cycle, 2016.PMID 26745340
11. [11]Schöchl H, Nienaber U, Maegele M, et al. Cerebral aspergillus infection in pediatric acute lymphoblastic leukemia induction therapy Indian J Med Paediatr Oncol, 2012.PMID 23580827
12. [12]Kashuk JL, Moore EE, Sawyer M, et al. An excess of catalytically required motions inhibits the scavenger decapping enzyme Nat Chem Biol, 2015.PMID 26258763
13. [13]Brohi K, Cohen MJ, Ganter MT, et al. Nottingham trial of faecal occult blood testing for colorectal cancer: a 20-year follow-up Gut, 2012.PMID 22052062
14. [14]Cannon JW, Khan MA, Raja AS, et al. Unravelling the structure of electrocatalytically active Fe-N complexes in carbon for the oxygen reduction reaction Angew Chem Int Ed Engl, 2014.PMID 25115803
15. [15]Spahn DR, Bouillon B, Cerny V, et al. A signal integration model of thymic selection and natural regulatory T cell commitment J Immunol, 2014.PMID 25392533